COVID-19, Inflammation and HPA axis activity, and Risk for Psychopathology in Youth

出现了前所未有的心理健康危机，自杀想法和行为（STBs）激增 在青年人中，艾滋病毒/艾滋病流行之前就已存在，并因这一流行病而进一步加剧。研究表明，年轻人在 COVID-19感染后1-6个月因精神病诊断接受事件治疗的风险增加。风险 在感染者中，性病也会增加; COVID-19后的认知障碍也会增加。 甚至在感染后约4个月报告。除了发病率和死亡率增加外， 为减少传播所做的努力给儿童和家庭带来了额外的压力（例如，父母 失业、父母死亡、在线学习），这些都与精神病理学的发病率增加有关。 在年轻的时候。然而，我们对COVID-19感染对人类健康的独特贡献的了解有限。 青年精神病理学发病率和与风险有关的生物机制。调节失调 免疫反应，特别是增加IL-6，IL-1b，C-反应蛋白（CRP）和TNF-α及其mRNA 和低皮质醇是与COVID-19严重程度和精神病理学有关的常见生物学机制。 我们的目标是研究COVID-19感染对青年精神病理学发病率的影响;其影响 炎症和HPA轴标志物;并确定临床，认知，生物和心理社会 这些特征将有助于预测COVID-19感染后有精神病理学发病风险的青年。我们 建议招募12-17岁的青年，没有精神疾病或慢性疾病或慢性病史 感染者：1）过去一个月内感染COVID-19（COVID，n=200）; 2）无 在过去6个月内患有COVID-19、流感（IFV）或任何呼吸道感染（无COVID，n=200）;以及3）青年 在过去的一个月内IFV（IFV，n=100）。IFV小组将允许我们检查COVID-19或 一般来说，感染与风险有关。将在基线后3、6和18个月对受试者进行随访 并对精神和身体症状、认知功能、精神病理学事件进行评估;流行病 和非流行性压力因素;以及所有时间点的风险和保护因素。在基线、3个月和6个月时，我们 将测量炎症（细胞因子，炎症基因的mRNA）;并收集急性和慢性HPA轴 活动测量（头发皮质醇浓度，唾液皮质醇）。我们假设新冠病毒组会显示 增加精神病理学发病的风险，特别是抑郁症和焦虑症以及STBs， 非新冠病毒和试管婴儿组。他们还将表现出炎症增加，精神和身体 随着时间的推移，HPA轴活动和认知功能降低;这些反过来又会预测 精神病发作这项研究将促进我们对COVID-19感染对 青年精神病理学风险和风险中涉及的生物机制。结果也将扩大 其他类型的感染。这项研究对于我们为今后的流行病做好准备至关重要， 流行病，这是不可避免的，并在上升。

There has been an unprecedented mental health crisis and a surge in suicidal thoughts and behaviors (STBs) among youth that predated and was further exacerbated by the pandemic. Studies show that youth are at increased risk for incident treatment for psychiatric diagnosis 1-6 months following COVID-19 infection. Risk for STBs is also increased among individuals with infections; and cognitive impairment following COVID-19 is reported even ~4 months following infection. In addition to the increased morbidity and mortality, the mitigation efforts put in place to reduce transmission resulted in additional stressors on children and families (e.g., parental job loss, parental death, online schooling) and these were associated with increased rates of psychopathology in youth. However, we have a limited understanding of the unique contribution of COVID-19 infection on incidence of psychopathology in youth and the biological mechanisms implicated in risk. Dysregulations in immune responses, specifically, increased IL-6, IL-1b, C-Reactive Protein (CRP), and TNF-a and their mRNA and low cortisol are common biological mechanisms implicated in COVID-19 severity and in psychopathology. Our goals are to examine the impact of COVID-19 infection on incidence of psychopathology in youth; its impact on inflammation and HPA axis markers; and to identify clinical, cognitive, biological, and psychosocial characteristics that will help predict youth at risk for onset of psychopathology following COVID-19 infection. We propose to recruit youth, aged 12-17 years, without history of psychiatric disorders or chronic Illness or chronic infections who were: 1) infected with COVID-19 within the past month (COVID, n=200); 2) without history of COVID-19, influenza (IFV), or any respiratory infections in the past 6 months (no-COVID, n=200); and 3) youth with IFV within the past month (IFV, n=100). The IFV group will allow us to examine whether COVID-19 or infections in general are associated with risk. Participants will be followed at 3, 6, and 18 months after baseline and assessed on psychiatric and physical symptoms, cognitive function, incident psychopathology; pandemic and non-pandemic stressors; and risk and protective factors at all timepoints. At baseline, 3, and 6 months, we will measure inflammation (cytokines, mRNA for inflammatory genes); and collect acute and chronic HPA axis activity measures (hair cortisol concentrations, salivary cortisol). We hypothesize that the COVID group will show increased risk of onset of psychopathology, specifically depression and anxiety disorders and STBs, compared to the no-COVID and IVF groups. They will also show increased inflammation and psychiatric and physical symptoms over time; and reduced HPA axis activity and cognitive function over time; and these will in turn predict onset of psychopathology. This study will advance our understanding of the impact of COVID-19 infection on risk for psychopathology in youth and the biological mechanisms implicated in risk. The results will also extend to other types of infections. This study is essential to inform our preparedness efforts for future epidemics and pandemics, which are inevitable and on the rise.